HR & others, i had a few questions regarding cholesterol and hope you can help with your expert opinion. Or perhaps other members with cholesterol problems. I will ask my hep doc when i see him in a few weeks but was hoping for your insight on it.
My primary doc called this morning and was very concerned about my lipid profile that was done last week, my total cholesterol is in normal range at 188 (up slightly from 184 in june) along with my triglycerides normal at 130 (down from 200 in june). The concern in my HDL & LDL numbers, LDL 143 (up from 117 in june) & LDL 19 (down from 27 in june). Looking at the report there is also some other alarming info about particle size both being very high. Do you think someone with these cholesterol #'s should still start treatment with pegasys & riba? or would you treat the LDL & HDL before tx, during tx or not at all until after tx. i have boderline high BP and take micardis 40 mg, 1xday. this is the only med i take. i need your opinion about this as i have the peg & riba already and was going to start after the holidays. Now i do not know what to do and worried.
Iam not obese maybe 10- 20 lbs overweight and have lost weight since june and was watching my diet with some moderate exercise and was expecting these #'s to be better not worse on this latest test! Is there a correlation between cholesterol & HCV? Can HCV cause the cholesterol to be out of range and will they get better after tx? Is it more dangerous to treat HCV with the cholesterol #'s like mine? Sorry for all the questions and the long post. Thank You
Not trying to butt in, and I would really like to see HR's take on this too. But I've actually been deliberately taking action to increase my total cholesterol, and especially my LDL level, prior to and during my treatment (believe it or not). The reason I did, is because there's a compelling recent report (which I posted here months ago) which pretty strongly suggests a significantly increased SVR rate for those with high cholesterol, especially high LDL levels (LDL being the harmful form of cholesterol). It builds upon previous reports which allude to the same idea. Apparently the lipids have an inhibiting effect on the virons, making it more difficult for them to latch on to the host cell (if I remember the report properly, which I probably don't right now).
Anyway, have a look at it. Plus it would be great to get HR's take on this. Oh, and of course the idea of increasing LDL levels to unhealthy levels is something I only plan on doing during treatment...obviously otherwise it's very ILL advised! Gotta go pick up my pepperoni pizza now, cya!
"Pre-treatment LDL & T-Cholesterol Predict SVR in HCV+"
Thank you mremeet, this is exactly the proper paper for this question and it answers it to the extent it can be answered. The dependence of SVr on LDL levels is quite impressive and the mechanism behind it a reasonable explanation.
Thus copyman, during TX it might be actually good to have these not so low LDL levels. Your HDL levels (I think you missplelled these) are another issue. Currently there is no other way than Niacin ( not for patients with liver disease!) exercise, weight loss and some fibrates to increase HDL levels.
The one promising drug in development to raise HDL development, by Pfizer, after they spent ONE BILLION!! on it -Torcetrapib- was stopped a few days ago - terminated with a bang. Horrrible.
After SVR you need to have your Dr. and yourself do its best to normalize the dyslipidemia by all means available.
Thanks everyone who responded so far. mremeet, thanks for the link. rev can you please elaborate on your comment? HR, does hcv have a direct correlation with lipids and if it does would it be possible the lipids normalize if i attained svr? and when you say "After SVR you need to have your Dr. and yourself do its best to normalize the dyslipidemia by all means available" do you mean to even take the colesterol drugs that are bad for the liver? If i was lucky enough to svr could the cholesterol drugs still damage the liver? thanks again to everyone :-)
One more thing I forgot to mention, and this is strictly an anecdotal observation I've made - I've seen more than a few people state (both here and elsewhere) that while undergoing treatment, their cholesterol levels took a sizeable drop. And then they lament that their cholesterol returns to it's normal (higher) level when they concluded treatment. I *think* I recall jim mentioning this happening to him too. Jim if you're reading this, set me straight if I've not recalled your situation accurately (which is always a distinct possibility nowadays).
On the other hand I'm on treatment right now, and my cholesterol has never been higher (I made 280 a month ago). But then I switched from skim milk to whole, started eating pizzas, cheesesteak subs, fried clams, lotsa butter on my pancakes, and plenty of Ben and Jerry's (New York Chocolate Fudge). So, take it for what it's worth. But based on from what some others have told me, don't be surprised if your cholesterol actually goes down during treatment.
Interesting topic and perhaps you can give some insight into my lipid history.
Prior to tx my total cholesterol (TC) ranged from 190 to 230, mostly dependent on diet. On a very low fat diet (Pritikin) I was able to lower TC to 140 but since I am unable to stick to this diet for more than a few months, it's really academic. While TC was between 190-230, HDL was generally around 30-32. When on Pritkin HDL dropped to 28. My HDL is resistent both to exercise, weight and one recommended drink that we shall not discuss in this thread.
So...going into tx, I had cholesterol around 220 with a low HDL and LDL somewhere over 100. Two weeks into treatment my cholesterol was 150 and LDL around 80. I stayed with excellent numbers like these throughout the 54 weeks of treatment, getting my LDL down to around 60 at one point, in spite of the fact my diet was full of saturated fats, etc, much worse than what I ate before or after treatment.
One month after treatment my lipid profile unfortunatly reverted back to normal, actually worse than normal. TC a few weeks ago was 264, LDL calculated 193, Tri's 163, HDL 38. Previous post tx values were TC in the 240 range with higher tri's (in the 200's) and lower HDL's -- 30-32 range.
So...Lousy lipid profile pre treatment -- both diet (except extreme diet) and exercise resistent. Excellent lipid profile during tx with exception of HDL BUT worse that lousy lipid profile post treatment.
Question: By what mechanisims did my lipid profile get so much better on tx -- I'm assuming it's the interferon -- and why is it now worse than even pre-treatment? Just one thing -- don't suggest I take any more interferon to lower my TC :) Lastly, any comments on taking Statins now versus waiting until the one year point? Also, any comments on Red Yeast Rice Extract? My brother claims some success with it.
It is well known that HCV itself lowers Cholesterol by an unknown molecular mechanism and that SVRs typically have a substantial rise in Chol levels following TX because the virus is gone.
So after that we are back to the question how to lower LDL and raise HDL.
I would do all the non statin measures first - and I am not convinced that your diet is truly optimized yet, but we cannot discuss that here, intense exercise, weight loss, plant stannols management of preprediabetic conditions ( HBa1c??) and then carefully use statins. Liver conditions needs to be monitored using ALT, and it also depends where are you with your liver overall now post TX - from what I read it looks very good (for Jim).
Both your HDLs look pretty bad, but see above. The only other good outlook is the ApoEMilano and that might be reserved for patients that already suffered a cvd event.
I have experimented extensively with diet and come to the conclusion that unless I go on a highly restricted low fat diet (fat calories under 10% of total calories) I only get mariginal gains from eating "healthy". For example, if I go on a diet of mostly whole grains and vegetables with let's say salmon three times a week, my TC will still be high UNLESS I eliminate all "good" mono oils and substitute a less fatty fish for salmon -- in other words, unless I go on a strict Pritikin diet, which as you know has its detractors due to the fact that you get few good fats.
Same with exercise. The only exception was when I was on a strict (and calorie restricted) "Zone" diet -- 30, 30, 40 (protein, fat, carb calories) where I was able to get my TC down to 170 with both decent Tri's and a good (for me) HDL in the high 30's. The problem, however, with the Zone diet is that while my workouts were better, I was unable to think and write clearly and writing is my profession. I also had a rise in ALTs, possibly from the diet, possibly from the more intense workout.
So, assuming the above -- LDL exercise and diet resistant -- what options do I have other than Statins or a natural statin like Red Yeast Rice Extract? And, given the the theory about TC and HCV, why did my TC drop so dramatically during treatment?
It is a good idea to always test the CPK together with the ALT if you are "liver conscious" and do intense workouts. The ALT rise might be solely from the muscles.
Re other means to lower LDL before statins, we might need to talk directly as mentioned before, since any package of measures can only be described combined with the reasons and concepts behind them and how they rhyme with other health issues of a person. Not enough space or dialog possible here. Without any statin or drug I achieve below 70 for my LDL ( 120-130 for TC)and close to 60 for the HDL, with TG in the 60 and other measures like homocysteine below LLN. But it is a lot of effort and hard work combined with intense and elaborate lab testing.
Just to clarify, I do not have NAFLD (to my knowledge) but research suggests that NAFLD is potentially more harmful to the liver (in terms of fibrosis progression) than possibly even the virus itself. I was made aware of this mid-treatment by my NP and none of my doctors had mentioned this to me prior, even though I had a bad lipid profile. If HR, is still following this -- would you mind explaining why "CPK" for liver monitoring? Wasn't aware this was a liver-specific enzyme. Thanks again for all your help.
I'm one who has had persistently low ldl for years, maybe as far back as 25 years. Always in the range of 63. Doc were curious but made no connections to anything. First time on tx ldl went all the way to 105, but went back to its usual neighborhood following tx. I'm still not clear with any connection to hcv (33 years), early cirrhosis, tx or relapse
If you do intense workouts your ALT can be high becaue it is also released from muscles upon some damage there. CPK is not a liver specific enzyme at all, but it is quite muscle specific, so if you have a simultanous elevation of ALT and CPK after exercise, it likely does not mean that exercise was bad for your liver, but that you had your extra ALT released by the muscles.
It also would be a good idea to have an advanced lipid analysis for particle size and number and apolipoproteins plus lipoprotein small "a" etc by either NMR analysis or lipoproteinanalysis or better both means to see how well they coincide. Also lipids are only one part of the story, cardiac C-reactive Protein is important, homocysteine, fibrinogen, microalbumin ( yes for your CVD risk assessment!). And a duplex carotis scan and an abdominal aortic scan for atherosclerotic plaques.
When you combine all this risk analysis it will guide you to determine how agressive you should or need to work against upcoming CVD risk/disease.
There is no doubt that janedoe2 is a serious, honest, intelligent and vigorous person. What a writeup on the failure of science to understand fundamental realities like gravity or quantum mechanics, let alone how things work in biology.
Keeping an open mind is always important, particularly if it concerns treatment of a disease that can threaten your life.
Many important arguments raised here at all levels, mostly con.
If Dr. Franco has post homeopathy therapy neg PCRs of truly chronic HCVs it would be very remarkable. If he has a good heart as stated, he might be willing to talk about it, if the party on the other side has an open frendly attitude towards him. I would like to call him, talk to him, I have an Italian scientific interpreter actually available - aside from Jane herself - conference call would be good.
As a molecular biologist the knowledge that the HCv virus represents a complex selfdoubling machine in the Trillion number in the human body, particularly in the liver, represent a platform from which all thinking re its elimination must start. There has to be some interaction with the formation of this virus for any treatment even if it is only that the "natural defense mechanisms' are activated by it.
Any effect has to be mediated by molecular interaction and the belief that imprinted water can selectivly eliminate this HCv machine amids all the other biomolecules on hand is a priori so extremely unlikely that we are not dealing with it unless hard evidence is presented otherwise.
Meanwhile it is important not to raise false hopes that could prevent people, like Jane from treating with realistic means, particularly if she is advancing fast, something we dont know yet.
Some of this alternative treatment might also slow or halt fibrosis progression. Is homeopathy likely to be able to do that? I would doubt it, but like to be convinced otherwise.
HR Wrote: I would do all the non statin measures first
Statins (a group of off the shelf meds for lowering cholesterol levels) are a hot target in HCV development. While I think you all are well informed, I have to assume you must have some other objections against it - i would like just ask what this is?
There are now serious studies since july from Japan stating statins inhibit HCV Replication in vitro effectively, other retrospective analysis showed that thair safety profile makes their application in HCV patients should no more questionable than with other patient populations. (In another case study about two cases there was however autoimmun hepatitis induced.)
There took place end of october an FDA/NIH-organized conference just before AASLD meeting about regulatory issues, the anti-HCV potential of statins was mentioned there among the leading other drug options under development.
I (obstinate non-responder) am now considering taking preferably fluvastatin (off-label) despite the fact having no elevated cholesterol levels.
I need some search work to provide you with all these important links, I hope later on the day I'll the time for it....
SK: While I think you all are well informed, I have to assume you must have some other objections against it - i would like just ask what this is?
Thanks for posting on the recent statin work. I only became aware of these studies after completing treatment, and had I known about them prior to treating I might have indeed started taking stains for their potential in reducing viral replication as well of course in their LDL lowering potential.
At that time, I just assumed that while statins could reduce LDL cholesterol, they had no benefits to the liver -- indeed quite the opposite -- that statins were one of those non liver friendly drugs metabolized by the liver.
Thinking back -- even though the viral replication studies weren't out -- statins might have been beneficial in terms of preventing NAFLD (non-alcholic fatty liver disease) but I was unaware of that condition at the time, nor was it mentioned to me by any of my doctors.
Now that I'm SVR, statins no longer hold an interest in terms of viral replication, so the interest again is in lowering LDL. My only hesitation is that I would prefer a more "natural" approach as opposed to starting on another medication with all that entails including possible side effects. Still, unless I am able to improve my lipid profile soon by other means, I will probably be on Statins within a few months.
"Those who follow a Mediterranean-style diet tend to have higher HDL ("good") cholesterol levels. Similar to those who follow a Mediterranean diet, Arctic-dwelling Inuit - who consume high amounts of omega-3 fatty acids from fatty fish - also tend to have increased HDL cholesterol and decreased triglycerides (fatty material that circulates in the blood). In addition, fish oil supplements containing EPA and DHA have been shown to reduce LDL ("bad") cholesterol and triglycerides. Finally, walnuts (which are rich in ALA) have been shown to lower total cholesterol and triglycerides in people with high cholesterol."
In addition there are some hints that omega-3 fatty acids may help to protect the liver directly.
(Of course dietary substitutes do not have the power to cure a hepatitis!)
i also read this with some intrest till i read a more complete article on the study the concentration they used on lescol in this study was 6.7 umol/l to acheive their results as by their own admision a 40 mg dose would at steady state (4-6 weeks) would reach 0.6 umol/l this represents a 11x higher blod concentration . as you increase dose you increase sx of drug thus causing evelation of ast alt maybe rhabdomyolysis . maybe more studies at a lower are needed just my thoughts
How was the course of your LFTs ALT gamma GT, bili before, during and after the 88wk IFN treatment? I assume it was Pegasys 180mug/week. No Riba?
Diagnosis of AIH is difficult and often remains with a question mark. More so with no autoantibodies. So how has the IFN worsened the inflammatory activity? ALT rise, platelet drop?
How does your Dr. suggest to monitor further progression/regression of inflammatory activity, fibrosis, overall liver functionality?
LFTs, biopsies, Platelets, US? Frequency?
If there were antifibrotic measures available worth trying such monitoring would be key.
I am leaving towards the end of this wk for 10 days. We can continue after that.
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